Curcumol inhibits colorectal cancer proliferation by targeting miR-21 and modulated PTEN/PI3K/Akt pathways.

Abstract

AIMS:

The purpose of this study was to demonstrate how curcumol affected the expression of miR-21 and whether its effects on miR-21 was associated with the activation of PTEN/PI3K/Akt pathways in CRC cells.

MAIN METHODS:

MTT and xenograft assay were used to examine how curcumol inhibits colorectal cancer (CRC) cells' growth. Q-PCR and western blot analysis were employed to test the role of miR-21 in the inhibition of curcumol on proliferation and PTEN/PI3K/Akt pathways of CRC cells.

KEY FINDINGS:

We found that curcumol effectively inhibited CRC cells from proliferating via the PTEN/PI3K/Akt pathways and reduced expression of miR-21 both in vitro and in vivo. miR-21 mimics were found to decrease the protein level of PTEN and increase the expression of PI3K, phospho-Akt (p-Akt) and NF-κB, while miR-21 sponge (miR-21-SP) enhanced the expression of PTEN and reduced the activity of PI3K, Akt and NF-κB. Furthermore, miR-21-SP strengthened the role of curcumol in up-regulating PTEN and inhibiting PI3K/Akt pathways, but miR-21 reversed the effect of curcumol on the PTEN/PI3K/Akt pathways.

SIGNIFICANCE:

Our research demonstrated that curcumol reduced the proliferation of CRC cells through PTEN/PI3K/Akt by targeting miR-21 and miR-21 could be a target molecule of curcumol for CRC treatment.

• Authors: Haowei Liu, Juan Wang, Yexing Tao, Xumei Li, Jianli Qin, Zhun Bai, Bixia Chi, Wei Yan, Xu Chen
• Journal: Life sciences (Life Sci) Vol. 221 Pg. 354-361 (Mar 15 2019) ISSN: 1879-0631 [Electronic] Netherlands
• PMID: 30811964 (Publication Type: Journal Article)
• Copyright: Copyright © 2019. Published by Elsevier Inc.

Chemical References

• MIRN21 microRNA, human
• MicroRNAs
• Sesquiterpenes
• curcumol
• Phosphatidylinositol 3-Kinases
• Proto-Oncogene Proteins c-akt
• PTEN Phosphohydrolase
• PTEN protein, human

Topics

• Animals
• Apoptosis
• Cell Line, Tumor
• Cell Movement
• Cell Proliferation (drug effects)
• Colorectal Neoplasms (drug therapy, genetics)
• Gene Expression Regulation, Neoplastic (drug effects)
• Humans
• Mice
• Mice, Nude
• MicroRNAs (drug effects, metabolism)
• PTEN Phosphohydrolase
• Phosphatidylinositol 3-Kinases
• Proto-Oncogene Proteins c-akt
• Sesquiterpenes (metabolism, pharmacology)
• Signal Transduction
• Xenograft Model Antitumor Assays